Regulation of vulnerable plaque development by the heme oxygenase/carbon monoxide system

Plaque rupture and luminal thrombosis is the most common cause of coronary occlusion that leads to acute coronary syndromes. High-risk plaques, or vulnerable plaques, are defined as lesions that are prone to rupture, also known as thin cap fibroatheroma (TCFA), or lesions prone to erosion or with calcified cores. This review will focus mainly on the vulnerable plaque, which is thought to be the precursor of the thrombogenic or ruptured plaque. Heme oxygenase 1 (HO-1) protein expression is specifically increased in lesions with a vulnerable plaque phenotype resembling TCFAs and correlates with a rise in expression levels of intimal proinflammatory markers. Data from several human and animal studies imply an important function for HO-1 in the genetic regulation of early, as well as late atherogenesis, and plaque destabilization toward a vulnerable phenotype. Although a direct association between HO-1, vulnerable plaque development, and clinical outcome is for now missing, the correlations that have been reported for HO-1 and coronary artery disease point to a possible link.

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